Morphogenesis-regulated localization of protein kinase A to genomic sites in Candida albicans

BMC Genomics

Research Article

Prashant R Desai¹  Alida Schaekel²  Joachim F Ernst² 

[1] Department Biologie, Molekulare Mykologie, Heinrich-Heine-Universität, Düsseldorf, Germany;Department Biologie, Molekulare Mykologie, Heinrich-Heine-Universität, Düsseldorf, Germany;Manchot Graduate School Molecules of Infection, Heinrich-Heine-Universität, Düsseldorf, Germany;

关键词: Candida albicans;    Protein kinase A;    Tpk1;    Tpk2;    Efg1;    Morphogenesis;   

DOI  :  10.1186/1471-2164-14-842

 received in 2013-06-03, accepted in 2013-11-15,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundThe human fungal pathogen Candida albicans is able to undergo morphogenesis from a yeast to a hyphal growth form. Protein kinase A (PKA) isoforms Tpk1 and Tpk2 promote hyphal growth in a signalling pathway via the transcription factor Efg1.ResultsC. albicans strains producing epitope-tagged Tpk1 or Tpk2 were used in genome-wide chromatin immunoprecipitation on chip (ChIP chip) to reveal genomic binding sites. During yeast growth, both PKA isoforms were situated primarily within ORFs but moved to promoter regions shortly after hyphal induction. Binding sequences for Tpk2 greatly exceeded Tpk1 sites and did not coincide with binding of the PKA regulatory subunit Bcy1. Consensus binding sequences for Tpk2 within ORFs included ACCAC and CAGCA motifs that appeared to bias codon usage within the binding regions. Promoter residency of Tpk2 correlated with the transcript level of the corresponding gene during hyphal morphogenesis and occurred near Efg1 binding sites, mainly on genes encoding regulators of morphogenesis.ConclusionsPKA isoforms change their genomic binding sites from ORF to promoter regions during yeast-hyphal morphogenesis. Tpk2 binds preferentially to promoters of genes encoding regulators of cellular morphogenesis.

【 授权许可】

Unknown   
© Schaekel et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.